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Researchers describe how human blood stem cells transform themselves to repair injured animal hearts

troponin T, which meant that they were human-derived cardiac myocytes. "That is a high frequency of new cells after only two months," Yeh says. The total proportion of cells that expressed HLA was two percent, which meant that the other one percent were human endothelial cells, which they further identified with the VE-cadherin marker. The researchers used PCR analysis to confirm the HLA findings, and then they stained the cells so that the human X chromosome would show up in one color, and the mouse X chromosome would be highlighted in a different hue.

The majority (73 percent) of HLA-positive myocytes contained both human and mouse DNA, and about 24 percent contained only human DNA. This suggests, says Yeh, that the CD34+ stem cells "fused" with existing mouse myocytes, and that the few cells without mouse DNA "either differentiated, or lost the mouse X chromosome when dividing." Such fusion has been seen in the liver when that organ repairs itself, Yeh notes. "Cell fusion has been important for muscle growth. Myocytes fuse to form a muscle and the muscle regrows fused."

He also says that cells with both mouse and human DNA are not diseased or cancerous, and appear to perform as needed, although more confirmatory work is needed before "we can declare them absolutely normal.

"This paper shows that fusion is a predominant event in muscle cell generation, and it may work by allowing a cell to enter the cell cycle and divide and produce new progeny, but all of this is new and needs to be studied further," Yeh says.

Cells that line the many vessels of the heart, however, developed differently in this experiment, Yeh says. More than 97 percent of endothelial cells with a human X chromosome showed no evidence of mouse DNA, which means that, once in the heart, they transdifferentiate, or morph directly into endothelial cells. "This is a fairly straightforward process for a stem cell, which is destined to become certain types of cell,"
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Contact: Nancy Jensen
nwjensen@mdanderson.org
713-792-0655
University of Texas M. D. Anderson Cancer Center
15-Dec-2004


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